title: Positivity for islet cell autoantibodies in patients with monogenic diabetes is associated with later diabetes onset and higher HbA1c level.
abstract: OBJECTIVE
  Islet cell autoantibodies are associated with autoimmune insulitis and belong to the diagnostic criteria of type 1 diabetes mellitus. However, growing evidence suggests that autoantibodies are present in other types of diabetes. Here, we focus on the autoantibody incidence in Czech patients with maturity-onset diabetes of the young and analyse their functional relevance in terms of diabetes onset and control.
  
  
  METHODS
  Autoantibodies against glutamic acid decarboxylase (GAD) 65 and protein tyrosine phosphatase islet antigen 2 (IA-2) were measured in a cohort of 28 Czech patients with maturity-onset diabetes of the young, all confirmed by genetic testing. Selected clinical data were correlated to the status and kinetics of autoantibodies.
  
  
  RESULTS
  One quarter of patients with maturity-onset diabetes of the young examined (7/28; 25%) was positive for GAD or IA-2 autoantibodies. GAD autoantibodies were more prevalent (7/7) than IA-2 autoantibodies (1/7). The incidence of autoantibodies did not correlate with human leukocyte antigen status. The patients who were positive for the autoantibodies developed diabetes later than those who were autoantibody-negative, but had worse glycaemic control (increased HbA1c ). Expression of autoantibodies decreased with any improvement of diabetes compensation. Only one patient did not correspond to the above and displayed signs of combined signs of maturity-onset diabetes of the young and Type 1 diabetes.
  
  
  CONCLUSIONS
  The data suggest transient but highly prevalent islet cell autoantibody expression in Czech patients with maturity-onset diabetes of the young. The autoantibodies were found in patients with delayed diabetes onset, and in times of insufficient diabetes control. As improvement of glycaemic control was associated with a decrease in levels of autoantibodies, their presence may reflect the kinetics of β-cell destruction induced by causes other than autoimmune ones.
authors.affiliation: Charles University in Prague, Third Faculty of Medicine, Prague, Czech Republic.
authors.forename: J
authors.initials: J
authors.lastname: Urbanová
authors.forename: B
authors.initials: B
authors.lastname: Rypáčková
authors.forename: Z
authors.initials: Z
authors.lastname: Procházková
authors.forename: P
authors.initials: P
authors.lastname: Kučera
authors.forename: M
authors.initials: M
authors.lastname: Cerná
authors.forename: M
authors.initials: M
authors.lastname: Anděl
authors.forename: P
authors.initials: P
authors.lastname: Heneberg
mesh_terms: D000293:Adolescent; D000328:Adult; D017668:Age of Onset; D001323:Autoantibodies / Q000276:immunology*; D002648:Child; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology / Q000276:immunology* / Q000378:metabolism; D005260:Female; D005941:Glucokinase / Q000235:genetics; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006442:Glycated Hemoglobin / Q000378:metabolism*; D051538:Hepatocyte Nuclear Factor 1-alpha / Q000235:genetics; D051557:Hepatocyte Nuclear Factor 4 / Q000235:genetics; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8 / Q000276:immunology*; D055815:Young Adult
chemical_list: D001323:Autoantibodies; D005941:Glucokinase; D005968:Glutamate Decarboxylase; D006442:Glycated Hemoglobin; D051538:Hepatocyte Nuclear Factor 1-alpha; D051557:Hepatocyte Nuclear Factor 4; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; C496487:HNF1A protein, human; C496592:HNF4A protein, human; C517652:hemoglobin A1c protein, human